Archive \ Volume.13 2022 Issue 3

Immunity and Therapeutic Approaches against Coronavirus Disease 2019


Maha Mahfouz Bakhuraysah1*


1Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Taif University, Taif 21944, Saudi Arabia. 


The Coronavirus disease 19 (COVID-19) pandemic has resulted in considerable mortality and morbidity worldwide since identified in Wuhan in late 2019. It was named severe acute respiratory syndrome coronavirus 2 (SARS-CoV2), which is a causative agent of human respiratory tract infection. The detailed mechanism of host immune response and pathogenesis to this virus is not fully elucidated. In this review, we recapitulate the characteristics of immune pathogenies of SARS-CoV-2 infection based on the recent studies of SARS-CoV-2 and previous information on MERS-CoV and SARS-CoV infection that may contribute to disease severity and death. The pathogenesis of COVID-19 includes virus entry and replication, cellular and humoral immunity, cytokine storms, and immune evasion. We also discuss the current approved COVID-19 vaccines in Saudi Arabia; Pfizer-BioNTech (BNT162b2), Oxford-AstraZeneca (ChAdOx1 nCoV-19), and Moderna (mRNA-1273). Furthermore, we review the characteristics and the contraindication of vaccines, and the most effective clinical diagnosis for this virus to combat the infection of SARS-CoV-2.   

Keywords: Immune response, Coronavirus, SARS-CoV, MERS-CoV, SARS-CoV-2, Vaccine


Novel coronavirus disease 2019 (COVID-19), which is known as coronavirus-induced pneumonia, is a member of the family Coronavirdae named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). In December 2019, this virus developed in Wuhan, a city in the Hubei Province of China, then the World Health Organization (WHO) announced the Public Health Emergency of International Concern (PHEIC) at the end of January 2020. On 11th March 2020, COVID-19 is considered a pandemic disease that shares about 80% sequence identity with SARS-CoV-1 [1]. Therefore, SARS-CoV-1, SARS-CoV-2, and Middle East respiratory syndrome CoV (MERS-CoV) are known as highly pathogenic human coronavirus infections that cause high mortality and morbidity [2, 3]. Up to date, there are about 577,429,314 confirmed cases of COVID-19 around the world of which 547,241,709 (94.77%) were cured, 6,407,868 (1.11%) were dead and the rest patients were either stable with about 23,779,737 (4.12%) or in critical situation 41,677 (0.01%). In Saudi Arabia, there are approximately 808,419 confirmed cases of coronavirus disease, 792,842 (98.07%) of the Saudi population recovered, while 9,243 (1.14%) of them were dead. Pneumonia appears to be the most common serious manifestation of COVID-19, characterized by fever, dry cough, fatigue, myalgia, dyspnea with acute respiratory distress syndrome (ARDS), and lymphopenia [4-6]. The cellular immune response is a crucial component of the immune defense that can recognize and control intracellular SARS-CoV-2 infection. However, an immunological role for orchestrated acute mortality from patients with SARS-CoV-2 is not yet illustrated. Therefore, the purpose of this review is to deliver an overview of the immune pathogenesis and T-cell response of SARS-CoV-2 infection, as well as, recent clinical diagnosis, treatment, and therapeutic/prophylactic vaccines against COVID-19, hinging on the information of two types of coronavirus; MERS and SARS that may assist in designing the appropriate immune intervention for.


Immune Pathogenesis of SARS-Cov-2 Infection

Immune function is considered a vital defense mechanism against infectious invasive pathogens. To facilitate the recognition of this new infection, the immunological mechanism of SARS-CoV-1 and MERS-CoV need to be addressed, especially changes in peripheral T-cells, their subsets, and B-cells. Coronaviruses classically infect the upper respiratory tract, however, MERS-CoV, SARS-CoV, and SARS-CoV-2 infect the lower respiratory tract and lead to pneumonia, which can be fatal.


Coronavirus is enveloped by single-stranded (ss), positive-sense RNA viruses’ genome (26-32 kb). Two-thirds of the viral RNA open reading frame (ORF1a/b) encodes polyproteins that form the viral replicase transcriptase complex in MERS-CoV, SARS-CoV, and SARS-CoV-2. While, other ORFs on one-third of the genome encode four main structural proteins; spike (S), membrane (M), nucleocapsid (N), envelope (E), and other accessory proteins that do not participate in the replication of the virus [7] (Figure 1). Coronavirus  S-protein presents on the viral surface and this feature determines virus entry into the host cells-surface significantly, as angiotensin-converting enzyme 2 (ACE2) [8]. ACE2 is a receptor that binds to the envelope S glycoprotein of SARS-CoV-1 and SARS-CoV-2 [9, 10], dipeptidyl peptidase 4 (DPP4) for MERS-CoV, and CD209L for SARS-CoV [11]. This type I membrane protein (51), ACE2, are prone to viral infection by expressing on several cell types, such as heart, kidney, blood vessels, gastrointestinal tract, and lung alveolar type II epithelial cells [12]. After attachment to cellular receptor(s), enveloped SARS-CoV-1 requires membrane fusion to enter host cells at the plasma membrane [13]. Subsequently, the genomic RNA of the virus is released into the cytoplasm, then uncoated RNA is translated into two polyproteins, after which the sub-genomic RNA begins to transcript and replicate [7, 14]. As a result, these newly synthesized proteins insert into the endoplasmic reticulum (ER) membrane, and the Golgi apparatus and N are formed. Eventually, the newly formed virion is often seen inside vesicles, then fuses with the plasma membrane to secret it [3] (Figure 2).




Figure 1. SARS-CoV-2 Structure and gene map. A. the structure of SARS-CoV-2 form enveloped with a positive single-stranded RNA (ssRNA) virus with a genome size (of 26-32 kb). In the SARS-CoV-2 gene map, the 5’ terminal two-thirds of the genome open reading frame (ORF1a/b) encodes polyproteins, which form the viral replicase transcriptase complex. Other ORFs on one-third of the genome encode membrane (M), nucleocapsid (N), envelope (E), spike (S) protein, and other accessory proteins that do not contribute to virus replication.